Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An enzymatic activity of shuttle systems for reduction equivalents transport (malate-aspartate, glycerophosphate, lactate, glutamate and beta-hydroxybutyrate dehydrogenase) was studied spectrophotometrically in liver tissue of intact rabbits and animals with experimental atherosclerosis. Content of malate, oxaloacetate, glutamate, alpha-ketoglutarate, alpha-glycerophosphate, dihydroacetone phosphate, lactate, pyruvate, beta-hydroxybutyrate and acetoacetate were studied. In experimental atherosclerosis coordinated functioning of the enzymes, which participate in the utilization of the cytoplasmic NAD-H2 and the alteration in the ratio of reduced and oxidized metabolites in the systems, were found to be impaired.
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PMID:[The function of shuttle systems of liver extramitochondrial hydrogen transport in experimental atherosclerosis]. 0 20

The status of some dehydrogenases (succinate dehydrogenase, mitochondrial alpha-glycerophosphate dehydrogenase and beta-hydroxybutyrate dehydrogenase) was studied in the course of long-term oral administration of cholesterol to rabbits. The data obtained indicate that within the first weeks of cholesterol administration there was a decrease in enzymatic activity of the dehydrogenases under study that mirrored the impairment of energy function of mitochondria. After experiments were initiated, alimentary hypercholesterolemia led to imbalance of anabolism and catabolism bearing resemblance to the status of oxidative processes in the Krebs cycle. There is every reason to believe that such a complex of changes in the dehydrogenases during hypercholesterolemia is characteristic for the initial stages of atherosclerosis. Elimination of cholesterol from the body by single hemosorption results in a tendency towards making the circulating lymphocytes egress from hypoxia. It is inferred that study of enzymatic activity of dehydrogenases should be used for the diagnosis of and the assessment of therapeutic measures for atherosclerosis under experimental and clinical conditions.
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PMID:[Mitochondrial enzymes in circulating lymphocytes during hemosorption for experimental hypercholesterolemia]. 661 50

Trans unsaturated fatty acids are formed during hydrogenation of edible oils and their consumption in the United States has increased with increasing utilization of margarines. The effect of elaidic acid and trielaidin on atherosclerosis in cholesterol-fed rabbits were studied many years ago by Weigensberg and McMillan, who found these fatty acids to be significantly more hypercholesterolemic but not more atherogenic. Jackson et al. have found that trans fatty acids are not inordinately atherogenic in swine. We have fed rabbits semipurified, cholesterol-free diets containing either 3.2 or 6.0% of trans fatty acid. The diets were slightly hyperlipidemic but no more atherogenic than the control diet. We measured the activities of five hepatic enzymes (glucose-6-phosphatase, fatty acid synthetase, malate dehydrogenase, beta-hydroxybutyrate dehydrogenase, and monoamine oxidase [EC 1.4.3.4]). The diets affected only the activity of monoamine oxidase, which was lower in the livers of rabbits fed 6.0% trans fatty acid. Vervet monkeys were fed the same diets either for 1 year or for 6 months and then returned to the control diet for 6 months. The dietary manipulations had no effect on serum or lipid levels or aortic sudanophilia. Trans fatty acid levels of the serum reflected dietary concentration. Six months after cessation of feeding of the trans fat the levels of trans fatty acids in serum were virtually normal. Trans fatty acids appear to exert a hypercholesterolemic effect but do not influence aortic atherosclerosis in rabbits or aortic sudanophilia in vervet monkeys.
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PMID:Trans fatty acid effects in experimental atherosclerosis. 681 29

To test the effects of trans unsaturated fatty acids (t-FA) on atherosclerosis, lipidemia and enzyme activities, rabbits were fed a semipurified, cholesterol-free diet containing 40% sucrose, 25% casein and 14% fat for 5 months. Two experimental diets provided either 6% (high) or 3.2% (low) t-FA. The control group was fed a fat of composition similar to the two experimental diets but free of t-FA. Serum cholesterol and triglycerides were elevated in the rabbits fed 6% t-FA. Liver glycerides were also elevated in this group. The fatty acids of plasma, erythrocytes, epididymal fat, liver microsomes and liver mitochondria reflected the dietary composition. Levels of aortic atherosclerosis were identical in the three groups. There were no significant differences in activity of five hepatic enzymes: glucose-6-phosphatase (microsomal), fatty acid synthetase (cytosolic), malate dehydrogenase, beta-hydroxybutyrate dehydrogenase and monoamine oxidase (mitochondrial).
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PMID:Influence of trans unsaturated fats on experimental atherosclerosis in rabbits. 683 52

Ciprofibrate is a well-known drug used to normalize lipid parameters and fibrinogen in atherosclerosis patients. In laboratory rodents such as rats or mice, ciprofibrate exhibits peroxisome proliferator activity. However, to date, no clear alterations or side effects caused by ciprofibrate have been noted in humans. In order to further investigate such possible relationships, we studied the effects of sustained ciprofibrate treatment in jerboas (Jaculus orientalis). In these rodents, ciprofibrate does not induce hepatomegaly or promote liver cell DNA replication, confirming that this species more closely resembles humans than do rats or mice. The jerboas were treated daily with ciprofibrate at 3 mg/kg body weight for 4 weeks. Subcellular markers, clinical enzymes and enzymatic antioxidant defenses were then assessed. The results showed a strong decrease in peroxisomal catalase activity and an increase in the level of malondialdehyde (a stress biomarker). Moreover, ciprofibrate in vivo and in vitro inhibited D-3-hydroxybutyrate dehydrogenase, a mitochondrial enzyme of the ketone body interconversion that is important in redox balance (NAD+/NADH+H+ ratio). In conclusion, under these conditions, ciprofibrate induced alterations in the liver oxidative metabolism.
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PMID:Sensitivity of liver metabolism in jerboa (Jaculus orientalis) to ciprofibrate, a peroxisome proliferator. 2147 72